Journal of neurotrauma
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Journal of neurotrauma · Mar 2008
Interleukin-6 and nerve growth factor upregulation correlates with improved outcome in children with severe traumatic brain injury.
Secondary brain damage after traumatic brain injury (TBI) involves neuro-inflammatory mechanisms that are mainly dependent on the intracerebral production of cytokines. Interleukin-6 (IL-6) may have a role both in the pathogenesis of neuronal damage and in the recovery mechanisms of injured neurons through the modulation of nerve growth factor (NGF) biosynthesis. However, the relationship between IL-6 and NGF expression and the severity and outcome of TBI remains controversial. ⋯ Furthermore, IL-6 and NGF upregulation after injury was associated with better neurologic outcomes. Based on these findings, we posit that NGF expression is a useful marker of brain damage following severe TBI. Moreover, the early upregulation of both IL-6 and NGF, which correlates with a favorable neurologic outcome, may reflect an endogenous attempt at neuroprotection in response to the damaging biochemical and molecular cascades triggered by traumatic insult.
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Journal of neurotrauma · Mar 2008
Laminectomy and fusion after spinal cord injury: national inpatient complications and outcomes.
There is little information about national in-hospital complication rates, adverse outcomes, and mortality after spinal fusion for spinal cord injury (SCI). The National Inpatient Sample (NIS) was utilized to identify 31,381 admissions of acute spinal cord injured patients who underwent spinal decompression with laminectomy and/or fusion (lam/fusion) in the United States from 1993 to 2002. Multivariate analysis was performed to analyze the effects of patient and hospital characteristics on outcomes such as mortality, complications, and discharge disposition, which were then stratified by age, level, and type of injury. ⋯ Patients with >3 comorbidities also had an increased risk of mortality (odds ratio [OR] = 1.8). Alcohol abuse was the most common medical comorbidity (present in 12% of patients treated). This study represents the first major national estimate of in-hospital mortality and complication rates after nonoperative and operative treatment for SCI.
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Journal of neurotrauma · Mar 2008
Erythropoietin potentiates EDHF-mediated dilations in rat middle cerebral arteries.
The neuroprotective effects of exogenous erythropoietin (EPO) in animals and humans after brain injury may be afforded, in part, by the influence of EPO on cerebral arteries. We tested (1) if EPO itself is vasoactive and (2) if EPO enhances endothelium-mediated dilations, specifically those mediated by endothelium-derived hyperpolarizing factor (EDHF). Immunoblotting and reverse transcriptase-polymerase chain reaction (RT-PCR) were used to detect EPO receptor. ⋯ This study demonstrates that EPO can directly dilate rat MCAs via the endothelium, though not all vessels are responsive. Additionally, pre-treatment with EPO for 24 h in vivo potentiates endothelium-mediated dilations, specifically those mediated by EDHF. Thus, enhanced endothelium-mediated dilations may partially underlie the neuroprotective effects of EPO after brain injury.
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Journal of neurotrauma · Mar 2008
Traumatic axonal injury in the spinal cord evoked by traumatic brain injury.
Although it is well known that traumatic brain injury (TBI) evokes traumatic axonal injury (TAI) within the brain, TBI-induced axonal damage in the spinal cord (SC) has been less extensively investigated. Detection of such axonal injury in the spinal cord would further the complexity of TBI while also challenging some functional neurobehavioral endpoints frequently used to assess recovery in various models of TBI. To assess TAI in the spinal cord associated with TBI, we analyzed the craniocervical junction (CCJ), cervico-thoracic (CT), and thoraco-lumber (ThL) spinal cord in a rodent model of impact acceleration of TBI of varying severities. ⋯ Quantitative analyses demonstrated that the occurrence and extent of TAI is positively associated with the impact/energy of injury and negatively with the distance from the brainstem. These observations show that TBI can evoke TAI in regions remote from the injury site, including the spinal cord itself. This finding is relevant to shaken baby syndrome as well as during the analysis of data in functional recovery in various models of TBI.
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Journal of neurotrauma · Feb 2008
Late proton magnetic resonance spectroscopy following traumatic brain injury during early childhood: relationship with neurobehavioral outcomes.
We sought to extend previous research that demonstrates reduced neurometabolite concentrations during the chronic phase of pediatric traumatic brain injury (TBI) in children injured during early childhood. We hypothesized that young children with TBI in the chronic phase post-injury would have lower N-acetyl aspartate (NAA) metabolite concentrations in gray and white matter in comparison to controls. We also hypothesized that metabolite levels would be correlated with acute TBI severity and neurobehavioral skills. ⋯ Late NAA and Cr levels in the medial frontal gray matter and NAA levels in the left frontal white matter were strongly positively correlated with initial GCS score. Metabolite levels were correlated with some neurobehavioral measures differentially for children with TBI or OI. Some neurometabolite levels differed between the TBI and OI groups more than 1 year post-injury and were related to injury severity, as well as some neurobehavioral outcomes following TBI during early childhood.